Description

Oestradiol 17ß a ligand that binds transactivation factors to stimulate the genome. It has a long natural history of approximately 1.2 billion years as bread mold (Saccaromyces cervicae) managed to synthesise it through an aromatasedependent reaction. It has sustained over all these years the randomised eliminating trials of nature and has successfully been passed on to primates and humans. Furthermore, it is endowed with the fundamental function of regulating reproduction. As such, it is illogical
to consider it as a carcinogen, although such role has been assigned to its effects on the endometrium and the breast.
Direct translation of research from the effect of Oestradiol 17ß on cancer cell lines and cancer models in animals to human spontaneous breast cancer, has been unfortunate for women. The findings of oestrogen receptor expression dazed many clinicians and encouraged them to promote a presumptive carcinogenic role for Oestradiol 17ß in the breast. If oestrogen receptor expression were to determine that role, it would have been a disasterous course of events since almost all female tissues express the oestrogen receptor or one of its isoforms and women would have walked around with tumours riddle their tissues.
Having benefited women with oestrogen deficiency states for over 60 years, Oestradiol 17β has always been the focus of suspicion. The National Institute of Health, and not the monitoring committee, stopped the oestrogen-only arm (conjugated equine oestrogen; CEE) of the WHI study before its conclusion on grounds that it could not foresee any benefit in the prevention of heart attacks – the primary end point of that study, despite the fact that there was a reduction in the incidence of myocardial infarction in the 50-69 years old that was offset by the higher incidence in the older age group.¹ A recent publication showed that the incidence of thrombo-embolism was slightly higher in the oestrogen-only group but this incidence was much lower than those women who used
continuous combined CEE and MPA.
Most importantly, was the publication in JAMA, 12th April 2006,³ when the re-analysis of the oestrogen-only arm of the WHI showed that CEE compared to placebo protected against the risk of breast cancer by 19-29% including the ductal carcinomas. Moreover, CEE replacement therapy has been shown to be associated with less invasive cancers.
The dogma is shattered to the embarrassment of the FDA and other regulatory authorities that hastened to classify oestrogen as a carcinogen. These agencies rushed to the media and before the appearance of the data in the scientific journals to woo women from asking for this treatment and instructed doctors not to prescribe it except for the shortest required time and in the lowest dose tolerable. Whether these hurried reaction to the initial WHI’s poorly scrutinised report has its roots in health economics or in the poorly informed epidemiologists that steered these actions, is not known and perhaps does not
matter. What matters, is the education of women of the falsehood of the idea that oestrogen causes breast cancer in postmenopausal women and their enablement to make an informed health choice for healthy ageing.

1. Anderson, G. L., M. Limacher, A. R. Assaf, at al. (2004).
“Effects of conjugated equine estrogen in postmenopausal women with hysterectomy: the Women’s
Health Initiative randomized controlled trial.” Jama 291(14): 1701-12.<br>
2. Curb, J. D., R. L. Prentice, P. F. Bray, at al.
“Venous thrombosis and conjugated equine estrogen in women without a uterus.” Arch Intern Med
166(7): 772-80.<br>
3. Stefanick, M. L., G. L. Anderson, K. L. Margolis, at al. “Effects of conjugated equine estrogens on breast cancer and mammography
screening in postmenopausal women with hysterectomy.” Jama 295(14): 1647-57.